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Sci. Aging Knowl. Environ., 16 October 2002
Vol. 2002, Issue 41, p. nw143
[DOI: 10.1126/sageke.2002.41.nw143]

NOTEWORTHY ARTICLES

All Fat Is Not Created Equal

Stomach surplus hinders rodents' ability to use glucose

Mary Beckman

http://sageke.sciencemag.org/cgi/content/abstract/sageke;2002/41/nw143

Key Words: ACRP30 • resistin • free fatty acids • hyperinsulinemia

Abstract: Chubby bellies deprive their owners of more than a svelte figure, according to new research. Abdominal flab in middle-aged rats causes insulin resistance, a common precursor to diabetes that afflicts old people disproportionately. Removing the fat restores insulin function, suggesting that the condition develops because fat accumulates around the internal organs. The surgical procedure partially mimics calorie restriction, and the results might eventually help scientists design drugs that simulate this life-extending regimen.

As people age, they acquire beer bellies and love handles. Their bodies also lose the ability to absorb glucose from the blood, a condition called insulin resistance. Circumstantial evidence links insulin resistance to visceral fat, the blubber found in bellies, but not to subcutaneous fat, which molds love handles. Exercise reduces visceral fat preferentially and improves a person's capacity to maintain proper amounts of blood sugar (see "Insulin Pathway Takes a Jog"). In addition, calorie restriction--which prolongs the lives of rats, mice, and possibly monkeys--keeps visceral fat in particular at bay and sharpens insulin response. Researchers have debated whether visceral fat is a byproduct or the cause of insulin resistance.

To determine whether visceral fat plays a role in glucose uptake, Gabriely and colleagues cut out equivalent weights of visceral or subcutaneous fat from two groups of adult rats. After allowing the rats to recover, the group measured how well the rodents extracted glucose from the bloodstream. Middle-aged rats that lack visceral fat used glucose as well as intact young ones did, whereas older animals missing subcutaneous fat and chubby controls developed insulin resistance. The results suggest that visceral, but not subcutaneous, fat cripples insulin function.

The viscerally rarefied animals also sponged up blood sugar as efficiently as did calorie-restricted rats of the same age. The dieting animals retained about the same small amount of visceral fat as did the ones that had undergone tummy tucks, suggesting that the regimen might improve insulin function because it melts stomach fat. To determine how fat might alter glucose uptake, the researchers measured the production of blood-borne molecules that fat cells secrete. They found that removal of visceral fat caused subcutaneous fat cells to produce about two-thirds less of the messenger RNA templates for the appetite-controlling hormone leptin and TNF-{alpha}, a protein thought to block biochemical pathways triggered by insulin. This observation suggests that visceral fat causes insulin resistance by changing the output of molecules made by a wide range of adipose tissues.

"This is the first demonstration that I know of [to show] that removal of visceral fat fixes the resistance problem," says endocrinologist Michael Schwartz of the University of Washington, Seattle. Endocrinologist Robert Schwartz of the University of Colorado Health Sciences Center in Denver suggests that calorie restriction might alter metabolism by influencing the types of fat that calories build. If scientists can concoct interventions that block meals from turning into visceral fat, they might be able to reproduce the life-extending power of calorie restriction--but without the hunger.

--Mary Beckman

I. Gabriely, X. H. Ma, X. M. Yang, G. Atzmon, M. W. Rajala, A. H. Berg, P. Scherer, L. Rossetti, N. Barzilai, Removal of visceral fat prevents insulin resistance and glucose intolerance of aging: An adipokine-mediated process? Diabetes 51, 2951-2958 (2002). [Abstract] [Full text]

Citation: M. Beckman, All Fat Is Not Created Equal. Science's SAGE KE (16 October 2002), http://sageke.sciencemag.org/cgi/content/abstract/sageke;2002/41/nw143







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